In a healthy state, BTG2 is associated with maintaining a quiescent state of T cells, aligning with the functional characteristics of Tregs.[27] Moreover, SATB1 has been demonstrated to be closely associated with the development of Tregs.[28] In conclusion, our study reveals a potential mechanism wherein metabolic reprogramming of tumor cells drives the functional differentiation of Tregs. Here, BTG2 is linked to neoplasm.